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Author Topic:   molecular genetic proof against random mutation (1)
Mammuthus
Member (Idle past 6562 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 226 of 274 (20772)
10-25-2002 5:28 AM
Reply to: Message 225 by peter borger
10-24-2002 9:23 PM


Dear Dr Page,
Often I have the feeling that I am waisting my time here on this board. If you for instance started to look up the papers I refer to, it certainly would improve our discussion.
M: I and other start to feel the same way when you persist in the fallacy of non-random mutations. If your hypothesis is going to have any merit it will have to stand on being falsifiable, testable, and supported by data. Not by changing defintions to suit your hypothesis needs.
cheers,
M

This message is a reply to:
 Message 225 by peter borger, posted 10-24-2002 9:23 PM peter borger has replied

Replies to this message:
 Message 228 by peter borger, posted 10-25-2002 8:47 PM Mammuthus has not replied

Karl
Inactive Member


Message 227 of 274 (20775)
10-25-2002 5:48 AM


...some genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors. Consequently, a small fraction of human genes may not possess discernible orthologues within genomes of model organisms.
Random mutation and selection?
I don't think so, the odds are against it.
Translation - your personal incredulity is against it.

peter borger
Member (Idle past 7752 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 228 of 274 (20847)
10-25-2002 8:47 PM
Reply to: Message 226 by Mammuthus
10-25-2002 5:28 AM


Dear Mammuthus,
YOU SAY:
I and other start to feel the same (about wasting time on this board, pb) way when you persist in the fallacy of non-random mutations. If your hypothesis is going to have any merit it will have to stand on being falsifiable, testable, and supported by data. Not by changing defintions to suit your hypothesis needs.
my response:
I explained several times now what I understand as non-random mutations (nonrandom with respect to nucleotide and location, you call them hot-spots, I guess). I also concurred that presently there is no convincing scientific evidence for deterministic mutaions this so I don't use it to substantiate my hypothesis. And since I backed up my claims with several scientific papers (on 1G5 and mtDNA) I it's not a fallacy.
Besides, the discussion with Dr Page is on genes present in human not in apes and non-random deletion.
Best wishes,
Peter

This message is a reply to:
 Message 226 by Mammuthus, posted 10-25-2002 5:28 AM Mammuthus has not replied

Replies to this message:
 Message 230 by Peter, posted 10-30-2002 8:46 AM peter borger has replied

derwood
Member (Idle past 1962 days)
Posts: 1457
Joined: 12-27-2001


Message 229 of 274 (20941)
10-28-2002 10:47 AM
Reply to: Message 225 by peter borger
10-24-2002 9:23 PM


quote:
Originally posted by peter borger:
Dear Dr Page,
Often I have the feeling that I am waisting my time here on this board. If you for instance started to look up the papers I refer to, it certainly would improve our discussion.
Weeks and weeks ago I referred to a Nature paper on the gene in LCR16a region. You even commented on it, and now I have to inform you again on the same topic. But, for the purposes of discussion, you can find the reference in: Nature 2001, volume 413, pp514-519.
The paper is on the morpheus gene family and the authors conclude:
...some genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors. Consequently, a small fraction of human genes may not possess discernible orthologues within genomes of model organisms.
Random mutation and selection?
I don't think so, the odds are against it.
Best wishes,
Peter

Funny you should feel that way - YOU mentioned the LCR, THEn went on about a gene.
If YOU could keep your claims straight, then there would not be so much confusion.
I take it hten that you have conceded the point on the LCRs?
I will look at the Nature paper later.

This message is a reply to:
 Message 225 by peter borger, posted 10-24-2002 9:23 PM peter borger has not replied

Peter
Member (Idle past 1565 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 230 of 274 (21090)
10-30-2002 8:46 AM
Reply to: Message 228 by peter borger
10-25-2002 8:47 PM


quote:
Originally posted by peter borger:

I explained several times now what I understand as non-random mutations (nonrandom with respect to nucleotide and location, you call them hot-spots, I guess).

Hot spots do not fit the definition of non-random you have
stated above.
When a mutation occurs (i.e. a copy error) it may or may not
occur at a hot spot.
It is more likely (statistically), but not certain.
Your definition would require that the location of any copy error
on any copy can be predicted in advance -- it cannot, to the best
of my knowledge -- and thus is random by the definition of
non-random that you give.

This message is a reply to:
 Message 228 by peter borger, posted 10-25-2002 8:47 PM peter borger has replied

Replies to this message:
 Message 231 by peter borger, posted 10-31-2002 12:16 AM Peter has replied

peter borger
Member (Idle past 7752 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 231 of 274 (21152)
10-31-2002 12:16 AM
Reply to: Message 230 by Peter
10-30-2002 8:46 AM


Dear Peter,
Why don't you have look at the sequences of the 1g5 gene in drosophila subspecies or the mtDNA sequences in subspecies of ancient human. You will discover --like me-- that there are two types of mutations: random and non-random with respect to nucleotide and position. The latter will give the illusion of common descent. (also read mail #185). Why not look at these sequences for yourself, instead of reiterating that I am wrong. I guess, it has been overlooked, since usually DNA sequences of subspecies are not presented. I recommnend you to do a bit of research yourself and demonstrate that I am wrong. Back it up with scientific publications. Till now nobody showed me a study that rebuts my claim beyond doubt.
Best wishes,
Peter

This message is a reply to:
 Message 230 by Peter, posted 10-30-2002 8:46 AM Peter has replied

Replies to this message:
 Message 232 by Mammuthus, posted 10-31-2002 3:32 AM peter borger has replied
 Message 264 by Peter, posted 11-11-2002 7:41 AM peter borger has not replied

Mammuthus
Member (Idle past 6562 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 232 of 274 (21158)
10-31-2002 3:32 AM
Reply to: Message 231 by peter borger
10-31-2002 12:16 AM


quote:
Originally posted by peter borger:
Dear Peter,
Why don't you have look at the sequences of the 1g5 gene in drosophila subspecies or the mtDNA sequences in subspecies of ancient human. You will discover --like me-- that there are two types of mutations: random and non-random with respect to nucleotide and position. The latter will give the illusion of common descent. (also read mail #185). Why not look at these sequences for yourself, instead of reiterating that I am wrong. I guess, it has been overlooked, since usually DNA sequences of subspecies are not presented. I recommnend you to do a bit of research yourself and demonstrate that I am wrong. Back it up with scientific publications. Till now nobody showed me a study that rebuts my claim beyond doubt.
Best wishes,
Peter

**************************
Alas I have rebutted your claim repeatedly. Look at the distribution of mutations and you will get a normal distribution. There are lots of human population genetics studies. I have referenced them before. That you continue to deny they exist is your fallacy. The burden of proof is on you Peter. I study ancient DNA and I know the study you are referring to well (in fact a colleague of mine wrote a piece in Science demonstrating several technical fallacies in the study). In no way based on the ancient sequence could you then determine where the next mutation would occur in the next human lineage or in the next generation. If you found Mungo lakes fellow villager, you cannot tell me exactly where the mutations in his mtDNA would be. That a particular kind of mutation occurs more frequently(i.e. transitions) does not make it a non-random mutation. That all of your hypotheses are based on a deterministic mutation mechanism falsifies them a priori as what you claim is not observed.
Where exactly, not probably, will the next mutation occur in my HV1 region?

This message is a reply to:
 Message 231 by peter borger, posted 10-31-2002 12:16 AM peter borger has replied

Replies to this message:
 Message 233 by peter borger, posted 10-31-2002 5:28 AM Mammuthus has replied

peter borger
Member (Idle past 7752 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 233 of 274 (21163)
10-31-2002 5:28 AM
Reply to: Message 232 by Mammuthus
10-31-2002 3:32 AM


dear Mammuthus,
You say:
Alas I have rebutted your claim repeatedly.
I say:
No, you didn't rebut the 1G5 gene in drosophila and you didn't rebut the line up of non-random mutaions in ancient mtDNA. You only keep repeating yourself that I have to predict were and when the next mutation in your HV1 region will occur. I already did a prediction for that, but you are still not content. In the meantime i gave you the new definition of non-random mutations [science is about adapting hypotheses, isn't it?], since the concept of deterministic mutations is presently not proven. But evidence is at close hands (see Dr Page's mailing: Cairns excerpt. I invite also Dr Page to rediscuss this topic since I discovered some 'strange stuff' in this mailing).
You say:
Look at the distribution of mutations and you will get a normal distribution.
There are lots of human population genetics studies. I have referenced them before. That you continue to deny they exist is your fallacy.
I say:
What you fail to acknowledge is that there are two types of mutations: random and non-random, and added together they give the impression of randomness. Only in extreme cases one can observe them
seperately, since usually the are obscured by random muations. Still one can observe them in the 1G5 gene. It is proof that they exist
and all you do is deny it and present me data from which it is not immediately clear what the random and non-random muations are. But even in the mtDNA study I referred to it is clear (as pointed out). Furthermore, there is still the invitation to discuss this example in detail and I will show you where it violates evolutionism. It can be demonstrated that these data violate 1) common decent, 2) random mutation, and 3) molecular clock. Open a new thread for it, and I will once more beat evolutionism.
You say:
The burden of proof is on you Peter. I study ancient DNA and I know the study you are referring to well (in fact a colleague of mine wrote a piece in Science demonstrating several technical fallacies in the study).
I say:
Technical fallacies that gave rise to the wrong sequences? If not, the example still stands and your attemp to rebut are void. But now I get it, your colleague also discovered that the data violate evolutionism and therefore the study cannot be correct. Isn't that the way it works. If studies appear in the journals that violate the hype the studies are wrong? Is that it?
You say:
In no way based on the ancient sequence could you then determine where the next mutation would occur in the next human lineage or in the next generation. If you found Mungo lakes fellow villager, you cannot tell me exactly where the mutations in his mtDNA would be. That a particular kind of mutation occurs more frequently(i.e. transitions) does not make it a non-random mutation. That all of your hypotheses are based on a deterministic mutation mechanism falsifies them a priori as what you claim is not observed.
Where exactly, not probably, will the next mutation occur in my HV1 region?
I say:
And again you try it. How many times do I have to reiterate myself on non-random mutations and what the may implicate for evolutionism? There we go again. By non-random I mean with respect to nucleotide and position. They will give the illusion of common descent. I already presented scientific evidence for the existence of these mutations so what's the point? O, now I get it, it overturns the strongest molecular argument for commmon descent. Well, I could care less.
Best wishes,
Peter

This message is a reply to:
 Message 232 by Mammuthus, posted 10-31-2002 3:32 AM Mammuthus has replied

Replies to this message:
 Message 234 by Mammuthus, posted 10-31-2002 6:28 AM peter borger has replied
 Message 235 by derwood, posted 10-31-2002 11:54 AM peter borger has replied

Mammuthus
Member (Idle past 6562 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 234 of 274 (21167)
10-31-2002 6:28 AM
Reply to: Message 233 by peter borger
10-31-2002 5:28 AM


PB:
I say:
No, you didn't rebut the 1G5 gene in drosophila and you didn't rebut the line up of non-random mutaions in ancient mtDNA. You only keep repeating yourself that I have to predict were and when the next mutation in your HV1 region will occur. I already did a prediction for that, but you are still not content. In the meantime i gave you the new definition of non-random mutations [science is about adapting hypotheses, isn't it?], since the concept of deterministic mutations is presently not proven. But evidence is at close hands (see Dr Page's mailing: Cairns excerpt. I invite also Dr Page to rediscuss this topic since I discovered some 'strange stuff' in this mailing).
M: You have not provided one single piece of evidence for a deterministic (non-random) mutation Peter. That transitions occur more frequently than transversions is all you have shown...WOW big freaking discovery Peter...how many decades has this been known?!?
In what concievable way does this violate principles of molecular evolution???
I say:
What you fail to acknowledge is that there are two types of mutations: random and non-random, and added together they give the impression of randomness. Only in extreme cases one can observe them
seperately, since usually the are obscured by random muations. Still one can observe them in the 1G5 gene.
M: I do not acknowledge your fairy tales. Where will the next mutation occur in 1G5 in the next generation? You cannot tell me that either much less for HV1. It is not a pre-determined mutation fate as you would wish to believe.
PB:
It is proof that they exist
and all you do is deny it and present me data from which it is not immediately clear what the random and non-random muations are. But even in the mtDNA study I referred to it is clear (as pointed out). Furthermore, there is still the invitation to discuss this example in detail and I will show you where it violates evolutionism. It can be demonstrated that these data violate 1) common decent, 2) random mutation, and 3) molecular clock. Open a new thread for it, and I will once more beat evolutionism.
M: If it is so easy do it here.
1) How does it violate common descent...surely you can show this in a few sentences
2) Show how it violates random mutation
3) I don't buy molecular clocks anyway because of the number of variables that can knock the clock off pace so go ahead and violate that one...it says nothing about the validity of evolution.
PB:
Technical fallacies that gave rise to the wrong sequences? If not, the example still stands and your attemp to rebut are void. But now I get it, your colleague also discovered that the data violate evolutionism and therefore the study cannot be correct. Isn't that the way it works. If studies appear in the journals that violate the hype the studies are wrong? Is that it?
M: Unwarranted conclusions prickly Peter
They failed to reproduce the ancient sequences in a separate laboratory and the sequence they got was most similar to an mtDNA pseudogene hence they have not discounted the possibilty that they have a modern DNA contamination. That is the flaw in the paper which was pointed out by Cooper et al. As to the analysis with regard to random mutations, that part is fine. It is only the origin of the Mungo lake sequence that is in doubt. And if it is a mtDNA pseudogene it is still of great interest to see how homologous sequences diverge under different selection regimes and with a different set of DNA repair enzymes affecting their respective mutation rates...but then you of course knew that there is a whole sub discipline that researches this topic didnt you?
PB:
And again you try it. How many times do I have to reiterate myself on non-random mutations and what the may implicate for evolutionism? There we go again. By non-random I mean with respect to nucleotide and position. They will give the illusion of common descent. I already presented scientific evidence for the existence of these mutations so what's the point? O, now I get it, it overturns the strongest molecular argument for commmon descent. Well, I could care less.
M: You have not Peter. You have failed to provide evidence of a deterministic mutation. You wish for it to be deterministic so you merely claim that higher transition than transversion frequency or the fact that dozens of prolines don't suddenly appear in most proteins is evidence of a deterministic process rather than selection against such mutation events or the freaking basic chemistry of nucleic acids i.e. C to T transitions. However, you have failed to demonstrate a mutation pre-adapting to an environmental pressure that does has not occurred yet, the organism then surviving due to that pre-emptive mutation and surviving i.e. Lamark. However, a large number of studies have shown that you can cause infrequent variants in the population to become frequent because of selection because those lacking said trait fail to pass on their genotype. Similarly, it is possible both experimentally and in the wild to see fixation by genetic drift....
Where is your evidence of a multipurpose Lamarkian genome? You keep claiming it is so easy to show this yet you have not answered most of my posts addressing your hypothesis, dodged Quetzals refutation of your W. nobilis example, and have otherwise repeated the same mantra over and over.
Answer here or start another thread as you see fit.
Cheers,
M

This message is a reply to:
 Message 233 by peter borger, posted 10-31-2002 5:28 AM peter borger has replied

Replies to this message:
 Message 238 by peter borger, posted 10-31-2002 9:28 PM Mammuthus has replied

derwood
Member (Idle past 1962 days)
Posts: 1457
Joined: 12-27-2001


Message 235 of 274 (21186)
10-31-2002 11:54 AM
Reply to: Message 233 by peter borger
10-31-2002 5:28 AM


PB:
"But evidence is at close hands (see Dr Page's mailing: Cairns excerpt. I invite also Dr Page to rediscuss this topic since I discovered some 'strange stuff' in this mailing). "
No you didn't. You just used that laughable creationist interpretation to try to claim the opposite of what the evidence indicates.

This message is a reply to:
 Message 233 by peter borger, posted 10-31-2002 5:28 AM peter borger has replied

Replies to this message:
 Message 237 by peter borger, posted 10-31-2002 9:10 PM derwood has replied

Fred Williams
Member (Idle past 4942 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 236 of 274 (21206)
10-31-2002 4:33 PM
Reply to: Message 220 by derwood
10-22-2002 11:48 AM


quote:
quote:
--------------------------------------------------------------------------------
YOU SAY:
No, if there were an intergenic locus of 5kb that showed no change between species in 20 million years, I would be a bit suspicious. But nothing in 300+ bps? Chance alone can probably explain that...
I SAY:
Chance alone? Calculate a bit on it, please. Demonstrate the odds.
-------------------------------------------------------------------------------
SLP: Mutation rate estimates are along the lines of 1 mutation per 10^9 bps per generation. At a 20 year generation time, that amounts to 1 million mutations in 20 million years. So any given site in a 3.2 billion bp genome has about a 0.03125% chance of 'suffering' a mutation in that time frame. That works out to less than 1 in 300 bases.
Very rough estimate and calculation, but it demonstrates my point.
ROTFL! Very ROUGH indeed! This is bogus beyond words. First, it’s 1 million generations, not mutations. Second, the rate you cite is way too low; your source must be either deleterious only, or rate/year, not generation. Estimates I’ve seen for *all* mutations (harmful through neutral through beneficial) runs at roughly 100 per diploid/generation, or 3 x 10^-8 bps/generation.
Finally, last and certainly not least, you assume a constant population size of 1 through that entire 20 million years! I didn’t realize we were asexual, and that there really was no Eve, ever. Just Adam, Adam Jr, Adam III, etc! ROTFL!
Granted this isn’t a straightforward computation. It’s an interesting problem. Here’s my rough estimate:
Let’s first try to calculate the number of organisms after 20 million years who should have a mutation at a specific neutral site. Assume 3x10^-8 bps/generation, and a population size of 1M. Also assume 20 year/generation. In 20 million years this is 1M generations. So, after 20 million years we will roughly have 3x10^-8 * 10^12 = 31,250 organisms with a mutation at a specific site. This is a rough estimate and will actually be lower because 1) duplicate hits are not accounted for, 2) it assumes the mutation is always inherited. Number 1 is negligible and can be ignored, number two however impacts the number by roughly 50% (due to mendelian genetics). So, that leaves 31,250/2 = 15,625. Out of a population of 1M, after 20 million years 1.6% have the mutation at a specific site.
Now we need to know what the odds are that 80 bps will avoid the mutation. This is given by:
P = 1 - [(100 — f)/100]^N, where f = frequency, N is number of attempts. In our example,
P = 1-[(100 — 1.6)/100]^80 = .725.
This means there is a 72.5% chance that at least one of the 80 neutral sites should have been mutated. Or, there is a 1 in 3.6 chance we would not see a mutation within the 80bp window.
For 300 sites, we get P = .992, or 99.2% chance, which means the odds are 1 in 125 we do not see a mutation within a 300bp window.
These odds obviously do not favor evolution, but they are also not near significant enough to declare the ZFX sequence anomaly a nail-in-the-coffin evidence against the theory. Still 1 in 125 chance IMO refutes your claim that chance alone can explain it. Maybe you got lucky, again. Evolution always gets lucky! LOL!
BTW, it does get really bad if the sequence were 5Kb. Better hope we don’t find one like that. The number becomes P = 9*10^-36!
[criticisms welcome — I went through this pretty fast]

This message is a reply to:
 Message 220 by derwood, posted 10-22-2002 11:48 AM derwood has replied

Replies to this message:
 Message 241 by derwood, posted 11-01-2002 1:54 PM Fred Williams has replied

peter borger
Member (Idle past 7752 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 237 of 274 (21221)
10-31-2002 9:10 PM
Reply to: Message 235 by derwood
10-31-2002 11:54 AM


dear Dr Page,
Is this an invitation to discuss the paper again?
Please let me know, and I will expose evolutionism as one big idee fix.
best wishes,
Peter

This message is a reply to:
 Message 235 by derwood, posted 10-31-2002 11:54 AM derwood has replied

Replies to this message:
 Message 239 by derwood, posted 11-01-2002 12:43 PM peter borger has not replied
 Message 240 by edge, posted 11-01-2002 12:56 PM peter borger has not replied

peter borger
Member (Idle past 7752 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 238 of 274 (21222)
10-31-2002 9:28 PM
Reply to: Message 234 by Mammuthus
10-31-2002 6:28 AM


Dear mammuthus,
Since this discussion is culminating in a "yes-it-is-no-it-isn't" debate, I like to have you a look at the 1g5 gene (#1 mail in the mol gen proof against random mut thread) and explain to me how you see this example. In my opinion it demonstrates non-random mutations with respect to nucleotide and position. If not, please explain your opinion in detail, so that you may be able to convince me. Next we can discuss the ancient mtDNA's or was the paper retracted by the authors? If not, the data still stand as scientific data, and your colleagues have to proof that their data are correct and not contaminations.
best wishes,
Peter

This message is a reply to:
 Message 234 by Mammuthus, posted 10-31-2002 6:28 AM Mammuthus has replied

Replies to this message:
 Message 242 by Mammuthus, posted 11-01-2002 2:35 PM peter borger has replied
 Message 249 by wj, posted 11-04-2002 8:22 PM peter borger has not replied

derwood
Member (Idle past 1962 days)
Posts: 1457
Joined: 12-27-2001


Message 239 of 274 (21268)
11-01-2002 12:43 PM
Reply to: Message 237 by peter borger
10-31-2002 9:10 PM


quote:
Originally posted by peter borger:
dear Dr Page,
Is this an invitation to discuss the paper again?
Please let me know, and I will expose evolutionism as one big idee fix.
best wishes,
Peter

Yes it is.
Your overconfidene is noted.
Common psychological trait among the pseudocertain.
Ask Fred.

This message is a reply to:
 Message 237 by peter borger, posted 10-31-2002 9:10 PM peter borger has not replied

edge
Member (Idle past 1792 days)
Posts: 4696
From: Colorado, USA
Joined: 01-09-2002


Message 240 of 274 (21269)
11-01-2002 12:56 PM
Reply to: Message 237 by peter borger
10-31-2002 9:10 PM


quote:
Originally posted by peter borger:
Is this an invitation to discuss the paper again?
Please let me know, and I will expose evolutionism as one big idee fix.
Hmm. I thought creationists always complained that evolution was too fluid to be (the ultimate) truth. Now you say that it is an idee fixe? Just how fixe'd do you think it is? Seems to me that evolution has changed to accomodated data. Just because it does not admit your interpretations does not mean that it is a rigid monolith.

This message is a reply to:
 Message 237 by peter borger, posted 10-31-2002 9:10 PM peter borger has not replied

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